Promotion of Lymphocyte Egress into Blood and Lymph by Distinct Sources of Sphingosine-1-Phosphate

Pappu, Rajita; Schwab, Susan R.; Cornelissen, Ivo; Pereira, João P.; Regard, Jean B.; Xu, Ying; Camerer, Eric; Zheng, Yaowu; Huang, Yong; Cyster, Jason G.; Coughlin, Shaun R.

doi:10.1126/science.1139221

Cited by 800 publications

(947 citation statements)

References 26 publications

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“…Most research on lymphocyte egress from DLNs has been carried out in homeostatic conditions and focused either on mechanisms that lymphocytes use to reach efferent lymphatic vessels, including regulation of CCR7 (7) and sphingosine 1-phosphate receptor-1 (S1P1) expression (18,29,30,53,54), or on mechanisms operating at the level of lymphatic endothelial barriers (31,55). We showed that the expansion of cortical and medullary sinuses in the late phase of inflammation functionally supports the egress of naive lymphocytes from LNs.…”

Section: Discussionmentioning

confidence: 91%

Expansion of Cortical and Medullary Sinuses Restrains Lymph Node Hypertrophy during Prolonged Inflammation

Tan

Yeo

Wong

et al. 2012

The Journal of Immunology

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During inflammation, accumulation of immune cells in activated lymph nodes (LNs), coupled with a transient shutdown in lymphocyte exit, results in dramatic cellular expansion. Counter-regulatory measures to restrain LN expansion must exist and may include re-establishment of lymphocyte egress to steady-state levels. Indeed, we show in a murine model that egress of lymphocytes from LNs was returned to steady-state levels during prolonged inflammation following initial retention. This restoration in lymphocyte egress was supported by a preferential expansion of cortical and medullary sinuses during late inflammation. Cortical and medullary sinus remodeling during late inflammation was dependent on temporal and spatial changes in vascular endothelial growth factor-A distribution. Specifically, its expression was restricted to the subcapsular space of the LN during early inflammation, whereas its expression was concentrated in the paracortical and medullary regions of the LN at later stages. We next showed that this process was mostly driven by the synergistic cross-talk between fibroblastic reticular cells and interstitial flow. Our data shed new light on the biological significance of LN lymphangiogenesis during prolonged inflammation and further underscore the collaborative roles of stromal cells, immune cells, and interstitial flow in modulating LN plasticity and function.

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Section: Discussionmentioning

confidence: 91%

Expansion of Cortical and Medullary Sinuses Restrains Lymph Node Hypertrophy during Prolonged Inflammation

Tan

Yeo

Wong

et al. 2012

The Journal of Immunology

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“…Therefore, it is conceivable that tissue‐activated CD2 − CD25 + NK cells arriving in the LNs also egress from the LNs through the efferent lymphatic vessel and circulate in a primed state in steady‐state conditions. T and B cells use sphingosine‐phosphate‐receptor 1 (S1P1) to egress from peripheral lymphoid organs;36, 37 however, down‐regulation of S1P1 through administration of FTY720, did not deplete NK cells from the circulation of mice or humans 38, 39. Consequently, it was demonstrated that NK cells express sphingosine‐phosphate‐receptor 5 (S1P5), which permits NK cell exit from the bone marrow and LNs in mice 40, 41.…”

Section: Discussionmentioning

confidence: 99%

Frequency and phenotype of natural killer cells and natural killer cell subsets in bovine lymphoid compartments and blood

et al. 2017

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SummaryNatural killer (NK) cells are widely distributed in lymphoid and non‐lymphoid tissues, but little is known about the recirculation of NK cells between blood and tissues. This is relevant to understanding recirculation in the steady‐state and also for determining the roles for NK cells in vaccine‐induced immunity and responses to infection. Therefore, the percentage of NK cells and their phenotype across peripheral blood, afferent lymph and lymph nodes in steady‐state conditions was investigated in cattle using the pseudo‐afferent lymphatic cannulation model. CD2+ CD25lo NK cells were the predominant subset of NK cells within the blood. In contrast, CD2− CD25hi NK cells were the main subset present within the skin‐draining afferent lymphatic vessels and lymph nodes, indicating that CD2− NK cells are the principal NK cell subset trafficking to lymph nodes via the afferent lymphatic vessel. Furthermore, a low percentage of NK cells were present in efferent lymph, which were predominantly of the CD2− subset, indicating that NK cells can egress from lymph nodes and return to circulation in steady‐state conditions. These compartmentalization data indicate that NK cells represent a population of recirculating lymphocytes in steady‐state conditions and therefore may be important during immune responses to vaccination or infection.

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“…3 Plasma S1P, which is present at the concentration of ~10 -6 M, is derived from erythrocytes, vascular endothelial cells (EC) and other cells. [4][5][6] Most of the biological activities of S1P are mediated by the S1P-specific G protein-coupled receptor family S1P 1~ S1P 5 . 7 Among these, S1P 1 , S1P 2 and S1P 3 are widely expressed major receptor subtypes.…”

Section: Introductionmentioning

confidence: 99%

Sphingosine-1-phosphate receptor 2 protects against anaphylactic shock through suppression of endothelial nitric oxide synthase in mice

Chen¹,

Okamoto²,

Yoshioka³

et al. 2013

Journal of Allergy and Clinical Immunology

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Promotion of Lymphocyte Egress into Blood and Lymph by Distinct Sources of Sphingosine-1-Phosphate

Cited by 800 publications

References 26 publications

Expansion of Cortical and Medullary Sinuses Restrains Lymph Node Hypertrophy during Prolonged Inflammation

Expansion of Cortical and Medullary Sinuses Restrains Lymph Node Hypertrophy during Prolonged Inflammation

Frequency and phenotype of natural killer cells and natural killer cell subsets in bovine lymphoid compartments and blood

Sphingosine-1-phosphate receptor 2 protects against anaphylactic shock through suppression of endothelial nitric oxide synthase in mice

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